Atopic dermatitis is a common severe skin disease usually seen in persons with personal or family history of allergic respiratory disease. The etiology is unknown, no satisfactory treatment exists and there is no distinct laboratory indicator of the condition. Various immune abnormalities have been demonstrated in atopic dermatitis. These include elevated serum IgE, depressed delayed cutaneous hypersensitivity and in vitro lymphocyte transformation and defective monocyte and granulocyte leukotaxis. These defects appear to fluctuate with the severity of the dermatitis. The diversity and transience of these abnormalities indicates a basic defect of differentiative and functional cellular regulation. Abnormal leukocyte responses to histamine and catecholamines in atopic dermatitis suggest possible molecular sites of dysfunction. This application proposes a prospective study in a large population of patients with well-defined atopic dermatitis and other inflammatory dermatoses. The major goals are: (1) definition of defective membrane receptor sites important in regulatory, inflammatory and immunologic events. (2) identification of distinct laboratory indicators of atopic dermatitis. (3) assessment of leukocyte responses to pharmacologic mediators in atopic dermitis. We will synthesize a tritiated H2-histamine receptor antagonist and will use it, along with a presently available radioligand specific for beta-adrenergic receptors, to characterize and quantify these receptors on various leukocyte subpopulations from patients with atopic dermatitis. Another segment of the proposal will test histamine and catecholamine effects on leukocyte adherence to provide a functional correlate for the radioligand studies. This assay has been shown to distinguish leukocytes from patients with atopic dermatitis and also offers a potential model for screening of pharmacologically active agents which might be therapeutically active in atopic dermatitis and other skin conditions.